Preferential campesterol incorporation into various tissues in apolipoprotein E3-Leiden mice consuming plant sterols or stanols
Abstract Intestinal absorption of plant sterols and stanols is much lower as compared with that of cholesterol; and therefore, serum concentrations are low. Circulating plant sterols and stanols are incorporated into tissues. However, hardly any data are available about tissue distributions of indiv...
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Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2008-09, Vol.57 (9), p.1241-1247 |
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Sprache: | eng |
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Zusammenfassung: | Abstract Intestinal absorption of plant sterols and stanols is much lower as compared with that of cholesterol; and therefore, serum concentrations are low. Circulating plant sterols and stanols are incorporated into tissues. However, hardly any data are available about tissue distributions of individual plant sterols and stanols, particularly in relation to their serum concentrations. We therefore fed female apolipoprotein E*3-Leiden mice a control diet, a plant sterol–enriched diet (1g/100 g diet), or a plant stanol–enriched diet (1g/100 g diet) for 8 weeks. In the sterol group, serum cholesterol-standardized campesterol and sitosterol concentrations were, respectively, 8 and 7 times higher as compared with those in the control group. Consequently, the serum campesterol-sitosterol ratio remained essentially unchanged. Cholesterol-standardized plant sterol concentrations increased significantly in all analyzed tissues, except brain. However, the campesterol-sitosterol ratio also increased in all tissues (except in liver and spleen), suggesting that campesterol is preferentially incorporated over sitosterol in those tissues. For the stanol group, serum plant stanol concentrations also increased; but the increase was but less pronounced. We conclude that, in apolipoprotein E*3-Leiden mice, campesterol is preferentially incorporated into most tissues over sitosterol, which cannot be deduced from changes in serum concentrations. |
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ISSN: | 0026-0495 1532-8600 |
DOI: | 10.1016/j.metabol.2008.04.018 |